Intermittent airway obstruction during sleep, or obstructive sleep apnea, occurs commonly in infants, children and adults. Repetitive episodes of obstructive apnea and resultant asphyxia may cause neurologic dysfunction, cor pulmonale and sudden death. The most comprehensive hypothesis to explain such intermittent airway obstruction is that the pharynx obstructs whenever the collapsing force of negative pharyngeal pressure exceeds the dilating force of genioglossus (GG) muscle contraction which pulls the tongue out of the pharyngeal airway. In the anesthetized rabbit we have previously demonstrated that GG electromyographic activity (EMG) increases with inspiration, hypoxia, hypercapnia and arousal, and decreases with general anesthesia and with pulmonary stretch receptor inhibition. Utilizing electromyographic and physiologic techniques in anesthetized and unanesthetized rabbits we propose to further define the relation of pharyngeal muscular contraction to pharyngeal airway patency. GG and diaphragmatic (DIA) EMGs will be processed to give a signal proportional to the force of muscular contraction. In anesthetized adult rabbits, the effects of pulmonary stretch receptors on GG and DIA EMGs, the effect of GG contraction on pharyngeal airway resistance and the potential role of other pharyngeal muscles as accessory muscles of respiration will be evaluated. In unanesthetized rabbits we will define the normal patterns of GG activity as a function of sleep state, compare GG and DIA EMG responses to hypoxia and arousal from hypoxia and to hypercarbia and arousal from hypercarbia, and determine the effects of chloral hydrate and of respiratory stimulants, such as methylxanthines and progesterone, on GG and corresponding DIA EMG activity. The data from these experiments should considerably expand our understanding of physiological and pathological mechanisms affecting maintenance of pharyngeal airway patency.